Segura J J, Calvo J R, Guerrero J M, Jimenez-Planas A, Sampedro C, Llamas R
Department of Dental Pathology and Therapeutic, School of Dentistry, University of Seville, Spain.
J Endod. 1997 Apr;23(4):205-8. doi: 10.1016/S0099-2399(97)80046-5.
The disodium salt of ethylenediamine tetraacetate (EDTA) is a calcium ion chelator used in endodontics to enlarge root canals. This study investigated the effect of EDTA on substrate adherence capacity of rat inflammatory macrophages to determine if EDTA leakage to periapical tissues during root canal therapy can alter macrophage function. Inflammatory macrophages were obtained from Wistar rats and resuspended in RPMI-1640 medium. Substrate adherence capacity assays were carried out in Eppendorf tubes for 15 min of incubation at 37 degrees C in a humidified atmosphere of 5% CO2. The adherence index (AI) was calculated. Results showed that EDTA decreased substrate adherence capacity of inflammatory macrophages in a time and dose-dependent manner. The lowest EDTA concentration that caused a significant inhibition of AI was 50 mM (p < 0.05), and the EDTA concentration that caused half-maximal inhibition (IC50) was 194 +/- 20 mM (p < 0.01). Calcium chloride (10 mM) increased the adherence index of macrophages by 17.1% (p < 0.05) and decreased the EDTA inhibitory effect on AI by 49.5% (p < 0.05). We conclude that an EDTA concentration lower than that used in endodontics decreased the substrate adherence capacity of macrophages significantly. Adhesion is the first step in the phagocytic process and in antigen presentation, but leakage of EDTA to periapical tissues during root canals preparation may inhibit macrophage function and reduce periapical inflammatory reactions.
乙二胺四乙酸(EDTA)二钠盐是一种钙离子螯合剂,用于牙髓病学中扩大根管。本研究调查了EDTA对大鼠炎性巨噬细胞底物黏附能力的影响,以确定根管治疗期间EDTA渗漏至根尖周组织是否会改变巨噬细胞功能。从Wistar大鼠获取炎性巨噬细胞,并将其重悬于RPMI-1640培养基中。在Eppendorf管中于37℃、5%二氧化碳的湿润气氛中孵育15分钟进行底物黏附能力测定。计算黏附指数(AI)。结果显示,EDTA以时间和剂量依赖性方式降低炎性巨噬细胞的底物黏附能力。引起AI显著抑制的最低EDTA浓度为50 mM(p < 0.05),引起半数最大抑制(IC50)的EDTA浓度为194±20 mM(p < 0.01)。氯化钙(10 mM)使巨噬细胞的黏附指数增加17.1%(p < 0.05),并使EDTA对AI的抑制作用降低49.5%(p < 0.05)。我们得出结论,低于牙髓病学中使用浓度的EDTA显著降低了巨噬细胞的底物黏附能力。黏附是吞噬过程和抗原呈递的第一步,但根管预备期间EDTA渗漏至根尖周组织可能会抑制巨噬细胞功能并减轻根尖周炎症反应。